Changes in pulmonary vascular resistance in response to partial liquid ventilation.
OBJECTIVE
Partial liquid ventilation (PLV) with perfluorocarbons decreases pulmonary vascular resistance (PVR) in injured piglet lungs without supplemental oxygen. These PVR changes may result either from direct mechanical effects or improved arterial oxygenation. In an uninjured hypoxic model of elevated PVR the authors asked the following questions: (1) Does prophylactic or therapeutic PLV ameliorate the PVR response to hypoxia? (2) Do prophylactic and therapeutic PLV have different PVR effects? (3) Does supplemental oxygen modify PVR response to PLV?


METHODS
Piglet (3 to 4 kg) lungs were isolated in situ without ischemia, hypoxia, or reperfusion injury. Pulmonary artery (PA) and left atrial (LA) cannulae were attached to a blood-primed extracorporeal membrane oxygenation (ECMO) perfusion circuit with a flow (QPA) of 80 mL/kg/min. Pressure-limited, volume-cycled ventilation (PIP < 25 mm Hg, Tv = 15 mL/kg) was initiated. PLV with perfluorodecalin (15 mL/kg) was administered endotracheally. Continuously monitored blood gas parameters allowed airway and extracorporeal adjustment of FiO2 to produce a PO2 appropriate to the experimental phase. PVR was calculated as (PPA - PLA/QPA). After a stable 30-minute normoxic baseline, animals were assigned randomly to three groups. In group I, control (n = 7), PVR was measured for 150 minutes in hypoxic lungs (FiO2 = 0.07, PPAO2 = 40 mm Hg, SPAO2 = 70%). In group II, prophylactic (n = 8), PLV was administered, followed by 90 minutes of hypoxia, and 60 minutes of oxygen recovery (FiO2 = 0.21-0.30, PPAO2 > 100 mm Hg, SPAO2 = 100%). In group III, therapeutic (n = 8), after 30 hypoxic minutes, PLV was administered and maintained for 90 minutes, followed by a 60-minute oxygen recovery phase. Results were expressed as mean +/- SEM. Statistical analysis of groups was performed by repeated measures of analysis of variance (ANOVA) and Tukey correction.


RESULTS
In group I normoxic gas-ventilated PVR was 174+/-12 mm Hg/L/kg/min. After 90 hypoxic minutes PVR was 318+/-37 (P < .01 vbaseline). In group II baseline PVR was 183+/-14. PVR after 30 normoxic minutes of PLV was 199+/-14 (P = ns v baseline). After 90 hypoxic minutes, PVR was 350+/-31 (P < .01 v baseline, and PLV alone) followed by a decrease to 192+/-19 after 60 minutes of oxygen recovery (P = ns v baseline or PLV alone). In group III baseline PVR was 160+/-17 and 325+/-29 after 30 hypoxic minutes. After 90 hypoxic minutes of PLV, PVR was 366+/-22 (P = ns v hypoxia control, P < .01 v normoxic baseline). PVR recovered to 189+/-19 after 60 minutes of oxygen recovery (P = ns v baseline).


CONCLUSIONS
Prophylactic/therapeutic PLV had no effect on hypoxia-induced increases in PVR and did not differ from each other. Although PLV alone decreases PVR in the injured lung without supplemental oxygen, elevated PVR associated with hypoxia was ameliorated only by supplemental oxygen in the liquid ventilated lung.
Lueders
M
M
Division of Pediatric Surgery, Columbia University, College of Physicians and Surgeons, and Babies and Children's Hospital of New York, Columbia Presbyterian Medical Center, New York 10032, USA.
Weiswasser
J
J
Aly
H
H
Stolar
C
C
D000818:Animals; D000831:Animals, Newborn; D005466:Fluorocarbons / Q000627:therapeutic use*; D000860:Hypoxia / Q000503:physiopathology / Q000628:therapy*; D008168:Lung / Q000098:blood supply*; D010952:Plasma Substitutes / Q000627:therapeutic use*; D011659:Pulmonary Gas Exchange / Q000502:physiology; D012121:Respiration, Artificial / Q000379:methods*; D013552:Swine; D014655:Vascular Resistance / Q000502:physiology*
D005466:Fluorocarbons; D010952:Plasma Substitutes; C008805:perfluorodecalin